The current study aimed to investigate whether the increased expression of long chain acyl-coenzymeA synthetase 1 (ACSL1) in peripheral blood leukocytes (PBL) may be a molecular marker for the genetic evaluation of acute myocardial infarction (AMI). The mechanism of action of ACSL1 in the pathogenesis of AMI was also investigated. A total of 75 patients with AMI and 70 individuals without coronary heart disease were selected to participate in the present study. The demographic and clinical information of the enrolled subjects was recorded. Reverse transcription quantitative polymerase chain reaction and western blot analysis were applied to measure the expression of ACSL1 at the mRNA and protein levels. It was demonstrated that the expression of ACSL1 mRNA and protein in PBL was increased in patients with AMI compared with controls. Logistic regression analysis indicated that ACSL1 expression in PBL was an independent risk factor of AMI. There was a significant positive association between the level of ACSL1 expression and the degree of atherosclerosis in the coronary artery. Furthermore, patients with AMI exhibited an increased risk of atherosclerosis due to increased fasting blood glucose, total cholesterol, triglyceride and lipoprotein levels and decreased high-density lipoprotein levels, compared with controls. Therefore, the current study demonstrated that ACSL1 expression was increased in the PBLs of patients with AMI. The elevated expression of ACSL1 acts an independent risk factor of AMI and may act as a potential biomarker when determining the risk of AMI.

Xuezhikang (XZK), an extract of red yeast rice, has been widely used for the management of hyperlipidemia and coronary heart disease (CHD); however, the effects of XZK treatment on kidney injury have not yet been fully identified. The aim of the current study was to evaluate the effects of XZK on the kidneys and investigate the related mechanisms in a rat model of hyperlipidemia. Thus, the effect on inflammatory transcription factors and kidney damage was investigated with in vitro and in vivo experiments on hyperlipidemic rats following XZK treatment. The results revealed that the plasma levels of total cholesterol (TC), triglycerides (TG) and low-density lipoprotein-cholesterol (LDL-C) were significantly decreased, while the levels of high-density lipoprotein-cholesterol (HDL-C) were significantly upregulated in the XZK treatment group, as compared with those in the hyperlipidemia group (P<0.05). In addition, the results demonstrated that XZK was able to repair the kidney damage caused by hyperlipidemia. Furthermore, the expression levels of the inflammatory transcription factors, tumor necrosis factor-α and interleukin-6, were shown to be reduced in the XZK group when compared with the hyperlipidemia group. In summary, XZK reduces kidney injury, downregulates the levels of TG, TC and LDL-C, as well as the expression levels of inflammatory transcription factors, and upregulates HDL-C. These results further the understanding of the molecular pathogenic mechanisms underlying hyperlipidemia and aid the development of XZK as an effective therapeutic agent for hyperlipidemia.

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